生物谷www.bioon.net 提要：中国农业大学、北京生命科学研究院（NIBS)、深圳作物热带亚热带分子设计育种中心以及堪萨斯州立大学的研究者联合报道了细菌毒性蛋白HopF2帮助病原细菌侵染植物宿主的机理。该研究发表于6月22日，国际植物学顶级杂志Plant Cell上。
引自NIBS官方新闻：效应蛋白是丁香假单胞菌致病的关键武器。细菌将这些蛋白“注射”到植物宿主细胞内，干扰植物的免疫信号通路以及其它细胞活动，使宿主易感。研究发现效应蛋白HopF2直接作用于拟南芥的激酶MAP kinase kinases（MKKs），并在后者的C末端Arg313饰以ADP-ribose。突变体分析表明HopF2与MKK的作用对前者的毒性功能必不可少。结果还揭示了MKK的C末端对其功能的重要作用。
本研究主要在北京生命科学研究所完成，研究获得了国家科技部863计划和北京市科委的资助。通讯作者唐晓艳博士为堪萨斯州立大学植物病理学副教授，同时在深圳作物热带亚热带分子设计育种中心从事研究工作。北京生命科学研究所周俭民实验室 王宇婧、李积凤、侯书国、王星玮等参与了研究工作。这是周俭民研究组继4月报道了一类寄主胞质内受体类似激酶是植物天然免疫信号传导的新的重要元件又一成果（详细内容：Cell Host & Microbe：PTI和ETI在进化上相互关联新证据）。（生物谷Bioon.net）
急需英才：北京生命科学研究所招聘周俭民实验室招聘职位
生物谷推荐原文出处：
The Plant Cell DOI:10.1105/tpc.110.075697
A Pseudomonas syringae ADP-Ribosyltransferase Inhibits Arabidopsis Mitogen-Activated Protein Kinase Kinases
Yujing Wang a,b, Jifeng Li b, Shuguo Hou b, Xingwei Wang b, Yuan Li c, Dongtao Ren c, She Chen b, Xiaoyan Tang d,e,1 and Jian-Min Zhou b
a College of Life Sciences, Beijing Normal University, Beijing 100875, China
b National Institute of Biological Sciences, Beijing 102206, China
c State Key Laboratory of Plant Physiology and Biochemistry, College of Biological Sciences, China Agricultural University, Beijing 100094, China
d Shenzhen Molecular Crop Design Center for Tropical and Subtropical Regions, Shenzhen 518040, China
e Department of Plant Pathology, Kansas State University, Manhattan, Kansas 66506
The successful recognition of pathogen-associated molecular patterns (PAMPs) as a danger signal is crucial for plants to fend off numerous potential pathogenic microbes. The signal is relayed through mitogen-activated protein kinase (MPK) cascades to activate defenses. Here, we show that the Pseudomonas syringae type III effector HopF2 can interact with Arabidopsis thaliana MAP KINASE KINASE5 (MKK5) and likely other MKKs to inhibit MPKs and PAMP-triggered immunity. Inhibition of PAMP-induced MPK phosphorylation was observed when HopF2 was delivered naturally by the bacterial type III secretion system. In addition, HopF2 Arg-71 and Asp-175 residues that are required for the interaction with MKK5 are also necessary for blocking MAP kinase activation, PAMP-triggered defenses, and virulence function in plants. HopF2 can inactivate MKK5 and ADP-ribosylate the C terminus of MKK5 in vitro. Arg-313 of MKK5 is required for ADP-ribosylation by HopF2 and MKK5 function in the plant cell. Together, these results indicate that MKKs are important targets of HopF2.
